In addition, a study showed that EETs extenuated insulin resistance via the PI3K/Akt signaling pathway in cultured bovine aortic endothelial cells (Wang et al., 2003), and Dhanasekaran et al. (2008) suggested that EETs were able to activate numerous targets of PI3K/Akt in a model of hypoxia/reoxygenation in primary cultured cardiomyocytes, such as an increase in PI3K activity and Akt phosphorylation. The gene discussed is AKT1; the disease is Insulin resistance.